Reperfusion is when the blocked artery is “unblocked” so that myocardial perfusion is restored (may not be to 100%). Severe ischaemia does not cause cell death instantly. It takes about 40 minutes, before reversible damage becomes irreversible. Reperfusion (i.e.: using thrombolytic therapy, or angioplasty, CABG) within 15-20 minutes after onset of ischaemia may prevent necrosis altogether. If done later, it may not prevent necrosis, but will salvage the ischaemic myocytes will necrose if nothing is done about them. Gross appearance is haemorrhagic because vasculature injured during ischaemic period starts leaking after reperfusion. Microscopically, you see exaggerated contraction of myofibrils in response to reperfusion .

Following an acute MI

• 2 mins after occlusion (REVERSIBLE)

  • loss of aerobic glycolysis, leads to inadequate ATP formation  accumulation of toxic products such as lactic acid. Ischaemia also has impact on contractility  this is lost.

• 15 mins after occlusion (REVERSIBLE)

  • Wrinkled fibres at infarct margin, and also electron microscopy shows mitochondrial swelling

• 15 hrs after occlusion (POINT OF IRREVERSIBLE DAMAGE)

  • Gross: dark mottling appearance, Light microscopy: coagulative necrosis, pyknosis of nuclei, myocyte hypereosinophilia, neutrophil infiltrates.

• 36hrs – 3 days

  • Gross: mottling with yellow-tan infarct centre with haemorrhagic border, Light microscopy: coagulative necrosis with loss of myocyte nuclei + striations, interstitial infiltrate of neutrophils.

• 7 days

  • Gross: maximally yellow tan and soft centre, with depressed red-tan margins, Light microscopy: phagocytosis of dead cells, granulation tissue at margins

• 1-3 wks

  • Gross: gray depressed infarct progresses from border to core of infarct, Light microscopy: granulation tissue with neovascularisation + collage deposition, decreased cellularity.

• > 2 mths:

  • Gross: white scar, Light microscopy: dense collagenous scar

There are many complications, which will be discussed below in chronological order:

• 1-3 days

  • Arrhythmias: sinus bradycardia, sinus tachycardia, ventricular premature contractions, ventricular tachycardia, atrial/ventricular fibrillation, asystole, atrial flutter.

  • Pericarditis: usually develops after a transmural infarct (not subendocardial). It occurs due to migration of underlying myocardial inflammation to pericardial surfaces.

• 3-5 days

  • Myocardial rupture: myocardial inflammation causes weakening therefore 1) rupture of ventricular wall resulting in haemopericardium + cardiac tamponade (usually fatal), 2) ventricular septum rupture leading to left-right shunt, 3) papillary muscle rupture cause mitral insufficiency (Fig 13-10 pp 562). Other causes of mitral insuffiency is papillary muscle dysfunction due to ischaemia, LV dilatation (physically pulling mitral valve apart), ventricular wall necrosis nearby papillary muscle emergence.

• 5-10 days

  • Mural thrombus: local contractility problems (stasis) + endocardial damage = thrombus formation = potential thromboembolism.

• 10 days +

  • Contractile dysfunction: LV contraction impaired, causing hypotension, pulmonary vascular congestion 》interstitial transudation 》pulmonary oedema. If infarct causes 20-25% of ventricle size = abnormal ventricule function, uif 40%+ = cardiogenic shock.

  • Ventricular aneurysm: Anterseptal infarct heals by forming fibrotic tissue, which is thin. This paradoxically bulges during systole – causing an aneurysm .

• Ganglionic blockers act mainly at the primary nicotinic-type cholinergic receptor at sympathetic and parasympathetic autonomic ganglia.

  • Agents which are classified as ganglionic blockers are not included among those drugs which block neuromuscular junctions.

• One class of blocker produces a depolarization block: Nicotine could produce this effect.

• The second class of agents include hexamethonium & trimethaphan These agents either competitively block the receptor or block the open channel configuration.

• For essential hypertension, ganglionic blockers have been replaced by better drugs.

  • Ganglionic blockers may be used for initial blood pressure control in patients with dissecting aortic aneurysm because, in addition to reducing blood pressure, blunting of sympathetic responses reduce sheer forces at the tear.

Predominary Sympathetic or Parasympathetic Tone
Antatomical Site	Predominant Autonomic Tone	Effect of Ganglionic Blockade
Arterioles	Sympathetic-adrenergic	vasodilatation; increased peripheral blood flow; hypotension
Veins	Sympathetic-adrenergic	dilatation; blood pooling; decreased venous return; decreased cardiac output
Heart	Parasympathetic-cholinergic	tachycardia
Ciliary Muscle	Parasympathetic-cholinergic	cycloplegia (loss of accommodation)
Gastrointestinal Tract	Parasympathetic-cholinergic	reduced tone and motility; constipation; decreased secretions
Salivary Glands	Parasympathetic-cholinergic	Xerostomia (dry mouth)
Sweat Glands	Sympathetic-cholinergic	Anhidrosis (lack of sweating)

Getting to the ear drum…1 4

1. S

   Moving the auricle and tragus constitutes the “tug test”, and is painful in external otitis media, but not in otitits media. Touching behind the ear may be painful in the latter.

   elect largest ear speculum the canal will accommodate.

2. Position head so instrument can be used comfortably.

3. Examine the problematic ear last to avoid spreading.

4. To straighten canal, grasp auricle and pull firmly but gently upward, backward and slightly away from the head.

5. Grasping the handle between your thumb and index finger, brace yourself against the patient’s face using your other fingers, to ensure unexpected movements are followed (pencil grip).

6. Gently insert speculum, aiming slightly down and forward.

7. Inspect the ear canal as you enter for any discharge, foreign bodies, redness of the skin or swelling, note cerumen may interfere with your view.

8. Inspect the ear drum.

Examining the ear drum…2

1. Inspect the eardrum, noting color and contour, the cone of light is useful in orientation.

2. Identify the handle of the malleus and inspect the short process of the malleus.

3. Gently move the speculum to see as much of the drum as possible.

4. The tympanic membrane consists of the pars tensa and pars flaccida, the malleus handle is in the middle of the tensa, superior to this is the lateral process of the malleus, the most easily recongnizable structure. The tip of the handle inferiorly is the umbo with the light reflex normally extending from this.

5. Identify handle, if not present look for the lateral process. Inspect the pars tensa systematically, starting in the posterior superior quadrant and moving forward, downward and backwards. Carefully inspect the pars flaccida.

Useful questions to ask yourself…2

1. Can the external canal clearly be visualized? If filled with debris is it safe to remove this material? If ear is possibly perforated, patient should be referred to ENT.

2. Can the TM and handle of the malleus be seen? Handle gives an idea of where the TM should have been if missing.

3. Is the TM intact? Note the difference between a retracted ear drum and perforation. If there is debris around the pars tensa or over the flaccida, patient may have a cholesteatoma, refer to ENT.

4. Is the TM the right color/transparency? Gold/blue/dull membrane indicates fluid in the middle ear. White patches are tympanosclerosis. Chalk patches and thick patches from prior surgery are not clinically important unless hearing is affected.

Common Problems…2

1. Unable to see properly? Check light and ensure battery is charged.

2. Red drum is all that is visible? Most likely posterior canal wall, try tilting otoscope anteriorly/superiorly or pulling the pinna further.

3. Anatomy is very abnormal? Start by looking for the lateral process of the malleus. Normally this is present despite other processes occurring in ear, orient yourself with it.

4. Is that a perforation? Usually obvious, however deep retractions can look similar. Blood vessels in the middle ear mucoas confirm the presence of a perforation. ENTs will often use pneumatic otoscopes to better evaluate this.

Normal TM Retracted TM Serous Otitis TM Cholesteatoma Perforated TM Ear Tube in place

Clinical Examples of Tympanic Membranes…3

References

1Bickley, Lynn S. Bates’ Guide to Physical Examination and History Taking: Eight Edition. Lippincort Williams and

Wilkins, 2003. 156-7.

2”Photographs of Ear Tubes, Eardrums, Infections, Cholesteatmas, and Acute Otitis Media.”

http://www.entusa.com/eardrum_and_middle_ear.htm. Accessed June 4, 2007.

3”How to Use an Otoscope.” http://www.comdis.wisc.edu/staff/mrchial/howotoscope.htm. Accessed June 4, 2007.

4“External Ear.” http://www.infovisual.info/03/048_en.html. Accessed June 4, 2007.

1. General Features
1. transepithelial transport - nutrients must pass across the epithelial lining of the small intestine
2. active transport - most nutrients must be transported across membrane using ATP of the cells
2. Carbohydrate Absorption
• facilitated diffusion - glucose and galactose (coupled with active transport of Na+)
• "carrier molecule" has binding sites for both sugar and Na+; relies on Na+ gradient
3. Protein (Amino Acid) Absorption
• facilitated diffusion - amino acids and small peptides (coupled with Na+ active transport)
• "carrier molecule" has binding sites for both amino acid and Na+; relies on Na+ gradient
• food allergies - absorption of proteins in infant gut causes early immune reaction
4. Lipid Absorption
• micelles - tiny balls of fats that result from bile salt emulsification and "lecithin"
• contain cholesterol and fat-soluble vitamins
• diffuse through lipid bilayer of membrane
• chylomicrons - micelles combined with associated proteins within the cell; enter the lacteals of the lymphatic system
5. Nucleic Acid Absorption
• pentoses, nitrogen bases, phosphates - absorbed by similar processes as sugars and amino acids
6. Vitamin Absorption
• fat soluble - Vitamins A, D, E, K are absorbed by epithelial cells along with lipid micelles
• OLESTRA - will carry fat soluble vitamins out in feces with it
• water soluble - Vitamins B & C absorbed by diffusion
• Vitamin B12 - large and electrically charged, must bind with "intrinsic factor" before being taken into the cell by endocytosis
7. Electrolyte Absorption
• Fe and Ca - primarily absorbed in small intestine
• ferritin - sequesters Fe in intestinal cells
• transferrin - transfers Fe into circulation when need is present (menstruation)
• Vitamin D - facilitates Ca absorption
• Na - exchanged for sugars and amino acids
• Cl - absorbed into cells and exchanged for HCO3-
• K - absorbed into cells due to osmotic gradients
8. Water Absorption
• small intestine - 95% of water absorbed by small intestine following transport of solutes
• large intestine - absorbs remaining water before moving the chyme on to the rectum
9. Malabsorption of Nutrients
• impairment of bile or pancreatic juice release
• infections of the intestinal mucosa
• gluten enteropathy - "gluten" protein in grains damages the mucosa of the intestines

1. Enzymatic Hydrolysis ("water" "breaking")
• hydrolysis - a water molecule is added between two "monomers" of a complex organic molecule in order break it down into its component parts
2. Carbohydrate Digestion
• monosaccharides - "monomers" such as glucose, fructose, and galactose
• disaccharides - sucrose (table sugar), lactose (milk sugar), and maltose (grain sugar)
• polysaccharides - starch (grains), glycogen (muscle)
• carbohydrate hydrolyzing enzymes
• salivary amylase - produces "oligosaccharides"
• pancreatic amylase - in small intestine
• intestinal enzymes - dextranase & glucoamylase (> 3 sugars), maltase, sucrase, and lactase
• lactose intolerance - decreased ability to digest lactose in the diet (use "lactase" supplements)
3. Protein Digestion
• amino acids - the "monomer" components of protein
• stomach - pepsinogen -----> pepsin (low pH)
• small intestine
• enzymes that cleave throughout the protein
• trypsinogen ---------------> trypsin
• chymotrypsinogen ------> chymotrypsin
• carboxypeptidase (carboxyl end of protein)
• aminopeptidase, dipeptidase (amino end)

4. Lipid (Fat) Digestion
• lipid structure - glycerol + 3 triglycerides
• lipases - enzymes that break down lipids
• bile salts - "emulsify" fats in 1 micron "micelles"

5. Nucleic Acid Digestion
• pancreatic nucleases - break down DNA and RNA

1. Bacterial Flora
1. digest remaining carbohydrates
2. responsible for producing gas (flatus)
3. synthesize complex B vitamins and vitamin K
2. Digestion and Absorption
1. reclaim most of the water
2. reclaim some of the electrolytes (Na+ and Cl-)
3. Motility of the Large Intestine
1. haustral contractions - slow acting segmental motion; moves chyme from one segment to next
2. mass movements - peristaltic waves that move food to the rectum during/after eating
• diverticula - herniation of the mucosa through the wall of the colon sigmoidd colon)
4. Defecation
1. defecation reflex - when feces (stool) enters rectum, spinal cord reflex is triggered
• internal sphincter (involuntary)
• external sphincter (voluntary)
2. Valsalva's maneuver - contraction of diaphragm and abdominal muscles to increase pressure for defecation
3. diarrhea - too much water in the stool
4. constipation - insufficient water or fiber

The genitourinary tract is the second most common site for tuberculous infection after the lungs; almost always affects the kidneys during the primary exposure to infection but does not present clinically.

Tuberculosis of the kidneys usually spreads by a hematogenous route from pulmonary disease, although it occasionally may be secondary to tuberculosis of the GI tract or bone.

By the time of diagnosis of renal tuberculosis, the primary source of pulmonary infection may be inactive or calcified.

The initial renal focus is usually a small tubercle in the glandular and cortical arterioles. With the passage of time, these lesions progress to form necrotizing lesions.

Tertiary TB from kidneys:

• Ureteric involvement occurs as a descending infection secondary to kidney infection.

• Bladder tuberculous infection is almost always secondary to renal involvement.

• Tuberculosis of the seminal vesicles usually occurs as a result of hematogenous spread.

Male genital tuberculosis presents with epididymitis, hydrocele or a palpable testicular mass, and discharging scrotal or perineal sinuses.

Female genital tuberculosis presents with pelvic pain, menstrual irregularity, and sterility.

vocal cord – has two sides, true and false. ID by the epithelium. Stratified squamous non-keratinized is found in places that undergo wear and tear. It makes sense then that the true vocal cord will have this type of epithelium. It also has skeletal muscle underneath. The false vocal fold has respiratory epithelium (ciliated, pseudostratified columnar with goblet cells). There are also glands underneath.

• 
  

• Trachea – has hyaline cartilage, muscle, and respiratory epithelium

• Lung – Many alveoli, know the two cell types: type 1-squamous types that allows for gas exchange, type 2 dome shaped cells that produce surfactant. The dust macrophages are larger, darker and are often located at the corners of the septa. A terminal bronchiole has no cartilage in the wall. The alveolar duct is a space that goes between what looks like alveoli that are broken open.

• Kidney - know that the cortex is the area with the renal corpuscles in it. The medulla has just tubes. Be able to tell the difference between proximal and distal tubule, the proximal is “pinker and fuzzier” while the distal is more regular and has a larger lumen. Also don’t forget about *podocyte cell-which is a stupid cell that sticks out from the glomerulus. Also know the parietal layer of Bowman’s capsule which is the squamous lining. Make sure you know the *Macula Densa which is just a row of cuboidal cells within the distal tubule that lies right next to the glomerulus. This is a chemoreceptor.

• Bladder - just know that it has transitional epithelium (dome shaped cells and may be bi-nucleate)
  Compare ureter with seminole vessicle, fallopian tube, vas defrens. Just be able to identify those

• Epididymis - Pseudostratified columnar epithelium with stereocilia. Be able to ID organ

• Testes – has a unique epithelium. You will have to be able to tell the difference between the different cell types i.e. Sertoli, Leydig, spermatogonia etc. Use the Wheater’s atlas for that, it is very good. Also, know what hormones influence these cells i.e. FSH, LH

• Vagina – compare to esophagus, has no glands, also the cells in the epithelium (stratified squamous non-keratinized) look empty. This is because they are loaded with glycogen that is evacuated in the preparation.

• Cervix be able to ID, it has a region where the epithelium changes to stratified squamous non-keratinized

• Uterus – mucosa, endometrium, know the two different types of cells i.e. ciliated and secretory

• Prostate – compare to seminal vessicle, ID by concretions

• Pituitary gland – two different sides, the less cellular side with lots of black dots is the pars nervosa or posterior pituitary. Remember that this side is neural ectoderm in origin and no hormones are produced here (that is not hard to figure out considering that these are just axons and nerve terminals). The pink circles are the Herring bodies which stores the hormones-oxytocin and vasopressin (ADH). The other half is the anterior pituitary or the pars distalis. Remember that this part is oral ectoderm in origin (Rathke’s pouch). There are three cell types here, the gray ones are the chromphobes which don’t do much so who cares, the pink ones are the eosinophils and they secrete prolactin and growth hormone. The blue-ish ones are the basophils. Remember, “B-FLAT” which is “B” for basophil, “F” for FSH, “L” for LH, “A” for ACTH, “T” for TSH. If you remember that, you will always get the hormones straight.

• Adrenal gland - make sure you know the three regions of the cortex and what is produced there. Remember “salty sweet sex” (no I didn’t make that up) Outside

• Zona Glomerulosa - ”salty”-mineralocorticoids (aldosterone), Zone Fasiculata-”sweet”-glucocorticoids/cortisol, Zona Reticularis-”sex” for androgens. The medulla has the chromaffin cells, neural crest in origin. They take the place of the post-ganglionic sympathetic neurons and therefore they secrete norepinepherine and epinephrine.

• Thyroid - unique looking organ, shouldn’t be confused with any other. Make sure you know the follicles with the colloid material that contains TGB (thyroglobulin). In between the follicles you will find cluster of cells the parafollicular or “C” cells. These are neural crest in origin and secrete calcitonin.

• Esophagus-compare to vagina, has stratified squamous non-keratinized epithelium with esophageal glands (duh). The muscularis externa contains either skeletal, smooth, or a mixtures of both types of muscle depending upon where the cross-section is made

• Stomach-simple columnar epithelium that is all mucous secreting therefore is does not have goblet cells. It also has three layers of muscularis externa and a large area of gastric glands. Magnify the area of the gastric glands and you will find the different cells types. *Parietal cell – pink, secretes HCL and intrinsic factor. *Chief cell – blue, makes pepsinogen. If you can’t remember which cell is which, just remember that the chief cells have a “manly” name and are therefore blue!
  Make sure you know the layers in all slides of the GI tract i.e. Lamina propria, muscularis mucosae, submucosa and muscularis externa. Also, if he wants you to ID a cell type within the lamina propria it is most likely a lymphocyte or plasma cell (black dots). If you see any white spaces that form lines within the lamina propria/villi it is probably a lacteal (small lymphatic vessel)
  Don’t forget about the Myenterric or Auerbach’s Plexus which is the parasympathetic ganglia located in between the inner circular and outer longitudinal muscle layers of the muscularis externa throughout the GI tract.

• Duodenum ID by the *Brunner’s glands which secrete an alkali mucous, it also has villi and plica circularis with normal GI epithelium (simple columnar with goblet cells and brush border)

• Jejunum-*no Brunner’s glands, also has longer plicae. Don’t forget about good old *Paneth Cells that have the bright red granules and secrete lysozyme.

• Ileum-shorter plicae, many more goblet cells, peyers patches (lymphatic nodules that don’t have the normal GI tract epithelium over them. They instead have the M cells)

• Colon no villi, many more goblet cells

• Gallbladder ID by the really weird projections on the surface, also has simple columnar epithelium, no brush border etc.

• Parotid gland-only serous units

• Submandibular – mixed but predominantly serous

• Sublingual-mixed but predominantly mucous

• Don’t forget about ******Serous Demilune!!!!!!!!!

• Liver-unless he uses the pig liver, you will not really see the classic lobule etc. ID by the central vein and the unique appearance of the hepatocyte cells. Different from spleen and pancreas because it all essentially one color. Also, no lymphatic nodules in the liver. Don’t forget about the triad found at the corners of the liver lobule -hepatic artery, portal vein and bile duct

• Pancreas – looks like undercooked steak, has areas of lighter pink coloring which are the islets of Langerhan’s (endocrine). Red areas in between is the exocrine portion. ID this organ by its coloration also, no lymphatic nodules.

• Lymphatic nodules - *always B cells (remembering that will help you with all of the secondary questions), primary (no germinal center, has not been antigenically challenged), secondary (germinal center*-has been antigenically challenged therefore it contains plasma cells and memory B cells*). They are found in the lymph node, palatine tonsil, ileum, colon, and appendix

• Lymph node - ID by the lymphatic nodules which are located all around the outside (cortex), also it has a capsule and a sub-capsular (not sub-scapular) sinus. If you remember that lymphatic nodules are only B cells, and the lymphatic nodules are located in the cortex, then the cortex has B cells! Next, paracortex has T cells and then the medulla has B cells! (BTB)

• Palatine tonsil - ID by the lymphatic nodules that are located everywhere (vs. in the periphery in the lymph node) also, it has crypts

• Thymus-no lymphatic nodules * (duh, it only has T cells!) Darker area outside is the cortex, lighter area inside is the medulla. **Hassel’s corpuscles-pink circular things, made of degenerating epithelial-reticular cells. If you look at it on high magnification you see lots of lymphocyte cells (black dots) and the occasional pink cells which are the epithelial-reticular cells

• Spleen - ID by the lymphatic nodules (white pulp but actually stains blue?????) with a central arteriole. Remember that the white pulp, since it is nothing more than a lymphatic nodule has B cells but, the area immediately around the central arteriole, PALS has T cells* Everything else in between is the red pulp

• Appendix - circular thing with a lumen and lymphatic nodules all around it. If you look closer, you will see that is has GI tract epithelium (simple columnar with goblet cells and a brush border)

Blood platelets and the blood clotting factors have a complementary function in haemostasis.

This is shown clearly by the bleeding time. A small (5 mm) incision in the flexor side of the forearm (Ivy test; first apply a sphygmomanometer and inflate to 40 mm Hg), or a prick in the earlobe (Duke’s test), produce a small amount of bleeding. The time needed to stop the bleeding depends on the speed at which a platelet clot is formed. The bleeding time (normally 3-9 minutes) is longer with severe thrombocytopenia or with impaired blood platelet function. Patients with clotting disorders such as haemophilia do not have any petechiae because platelet adhesion and aggregation are sufficient to close small lesions.

The number of blood platelets is normally much more than is needed for haemostasis (normal platelet count 150,000-450,000/µl). If the platelet count is less than 20,000/µl, the haemorrhaging risk increases considerably. If the count is less than 5,000/µl haemorrhaging will almost certainly occur.

Thrombocytes survive for 10 days on average. Usually a third is sequestered in the sinusoids of the spleen. This percentage increases in case of splenomegaly, especially if this is attributable to a portal hypertension.

Hemopoiesis: process of red blood cell (RBC) synthesis.

Pluripotent stem cells differentiate  into ‘differentiated’ hemopoietic progenitors influenced by:

• Cytokines

• Transcription factors (TF)

• Epigenetic events

As differentiation occurs there is lineage commitment ( plasticity and self renewal capacity)  eventually the formation of mature RBC (or as dictated by the specific lineage).

Stem cells: are characterised by

• No lineage specific markers (CD34⁺, KIT⁺, CD38^-, Dr^-)

• Quiescence (low % in S phase)

Genetically marked hemopoietic stem cells can differentiate into many ‘lineage’ and eventually cell types:

• Skeletal

• Cardiac

• Hepatocytes

• Astrocytes

• Endothelial cells

• Epithelial cells

Bone marrow contains 3 populations of stem cells.

Cytokines: are proteins that modulate function, activity and number of various other cells, e.g.:

• Non-lineage specific: KIT ligand / stem cell factor and IL-3

• Lineage specific: G-CSF (used extensively in bone marrow transplant), GM-CSF, thrombopoietin and erythropoietin.

Transcription factors: are signalling molecules which control gene expression by binding to regulatory sequences (promoter & enhancer regions), e.g.:

• GATA-1: (erythroid development); if knocked out  no erythroid progenitors  severe anaemia

• PU1: (myeloid development); if knocked out  few early myeloid progenitors (numerous molecules, combination and dose all play a role)

• Ikaros (lymphoid development)

Alterations in levels of TF help determine lineage commitment of multipotent progenitor cells.

Epigenetic factors: genetic memory (for lineage) is not just a matter of transcription factors and cytokines: e.g.

• Chromatin accessibility: expressed regions of the genome have open chromatin (i.e. DNA is not double stranded allowing access by TF) – modulated by acetylated histones

• Methylation changes: methylation status of DNA can determine transcription of some genes

• Nuclear location: active and silent genes occupy different sub nuclear compartments (silent B globin genes located near heterochromatin as opposed to active B globin genes which is located away from heterochromatin)

• Replication timing: transcriptionally active regions are replicated in S phase

Others include CoA recruitment, transcriptional activation, TF recruitment, linker histones, histone remodelling and chromatin remodelling.

B globin gene fragments taken from cells at different stages of development  placed in host cells  show pattern of gene expression of donor (rather than host). Therefore the developmental stage expression is determined largely by the epigenetic template carried by the chromosome fragment (rather than that of the host cell).

Assessment of bone marrow function: many different measurements can be taken to assess the bone marrow:

• Peripheral blood counts (e.g. Hb, WCC & platelets) – crude

• Reticulocyte count (e.g. LDH & bilirubin) – useful for situations with  turnover (e.g. in haemolytic anaemia); gives an indication of erythropoiesis

• Haemoglobin electrophoresis (e.g. in thalassemia)

• Bone marrow biopsy

• CD34 enumeration; antigen for primate progenitors – common practical test for stem cell numbers.

• CFU assays

The serum ferritin test is ordered to see how much iron your body has stored for future use. Reduced serum ferritin concentration is the most useful test for diagnosis of iron deficiency.[1] As the body iron stores decrease so does the serum ferritin. A serum ferritin concentration below 12 ug/L is virtually diagnostic of absent iron stores.

On the other hand, a normal serum ferritin concentration does not confirm the presence of storage iron, because serum ferritin concentration may be increased independently of body iron by infection, inflammation, liver disease, malignancy, and other conditions.[2]

The goal of therapy in individuals with iron deficiency Anemia is not only to repair the Anemia, but also to replenish the iron stores. Sustained treatment for a period of 6 to 12 months after correction of the Anemia will be necessary.

The Hemoglobin concentration begins to increase after the first week and is usually normal within 6 weeks. Microcytosis may take as long as 4 months to resolve completely. The serum ferritin concentration remains below 12 ug/L until the Anemia is corrected and then gradually rises as storage iron is replenished.

References:
==========
1. Goddard AF, McIntyre AS, Scott BB: Guidelines for the management of iron deficiency anaemia. British Society of Gastroenterology. Gut 46(suppl 3-4):IV1, 2000.
2. Cook J: The nutritional assessment of iron status. Arch Latinoam Nutr 49:11S, 1999


normal serum ferritin concentration does not confirm the presence of storage iron, because serum ferritin concentration may be increased independently of body iron by infection, inflammation, liver disease, malignancy, and other conditions.[1]

An increased ferritin (>400 ng/ml) occurs in iron excess and in the following: iron overload from hemochromatosis or hemosiderosis; oral or parenteral iron administration; inflammatory diseases; acute or chronic liver disease involving alcoholism; acute myoblastic or lymphoblastic leukemia; other malignancies (Hodgkin’s disease, breast carcinoma, malignant Lymphoma); Hyperthyroidism; hemolytic Anemia, megaloblastic Anemia; thalassemia (normal or sometimes higher).

Ferritin is normally found mainly inside of cells, with only a small amount in the blood. When there is damage to organs that contain ferritin (especially the liver, spleen, and bone marrow), ferritin levels can become elevated even though the total amount of iron in the body is normal.

References:
==========
1. Cook J: The nutritional assessment of iron status. Arch Latinoam Nutr 49:11S, 1999.

Pathophysiology:

T vaginalis principally infects the squamous epithelium of the genital tract. Incubation time is generally between 4 and 28 days. Infection may persist for long periods in females, but generally persists less than 10 days in males. Anecdotal evidence suggests that asymptomatic infection may persist for months or even years in women.

In females, vaginitis is the most common manifestation of infection. Other complications include infection of the adnexa, endometrium, and Skene and Bartholin glands. Males are usually asymptomatic. When symptoms are present, they usually manifest as urethritis. Up to 11% of nongonococcal urethritis cases are caused by T vaginalis. Other complications include infection of the prostate, foreskin, glans, and epididymis.

Infection with T vaginalis is a marker of high-risk sexual behavior. Co-infection with other STDs is common. In one study of adolescents who had a diagnosis of at least one STD, there was almost a 9-fold increase in the likelihood of T vaginalis infection in the ensuing 3 months.

Infection produces immunity that at best is only partially protective. Evidence of lymphocyte priming is shown by the presence of antigen-specific peripheral blood mononuclear cells. An antibody response locally and in serum has also been detected. Despite the interaction that the human immune system has with T vaginalis, little evidence exists that it prevents infection. One study showed no association between trichomoniasis and the use of protease inhibitors or immune status in women with HIV. Another study showed that HIV seropositivity does not alter the rate of infection.


Vertical transmission of T vaginalis during birth is possible and may persist up to 1 year. From 2 to 17% of female offspring of infected women acquire infection.


Nitroimidazoles are a class of drugs used to fight a variety of parasitic and anaerobic bacterial infections. The drug is taken up by target organisms and reduced to its active form. The reduced drug then disrupts the helical structure of the DNA within these microbes preventing nucleic acid synthesis and eventually leading to cell death.


Metronidazole (Flagyl) -- Active against various anaerobic bacteria and protozoa; mode of action not well understood; appears to be absorbed into cells; intermediate-metabolized compounds formed bind DNA and inhibit protein synthesis, causing cell death.
Metronidazole is treatment of choice.
Single-dose therapy with 2 g PO is as effective as prolonged therapy with 500 mg bid for 7 d.
Single-dose therapy increases compliance.
Metronidazole gel is effective in less than half the cases of trichomoniasis.
Now reports of resistance to metronidazole approaching 5-10% exist.
If treatment with either single-dose or multi-dose therapy fails, patient should be treated with 500 mg PO bid for 7 d. If this fails, patient should take 2 g PO qd for 3-5 d

• Chlamydia is the commonest cause of PID.
  
• The risk of sterility is possibly as high as 15 - 20 % after a single attack.
  
• Gonorrhoea has been reported to be present in 14% of cases in a recent survey.
  

• As these patients will present with pelvic pain, perhaps with discharge, dyspareunia etc., ectopic pregnancy should be excluded by arranging an urgent beta-HCG.
  

• Antibiotic therapy must cover the range of possible infecting organisms and several drugs are the norm to cover the possibility of chlamydia, gonorrhoea, anaerobes etc.
• oral oflaxacin plus metronidazole for 14 days, both taken in a dose of 400mg. twice daily
• alternative regime is ceftriaxone 250mg. i.m. or cefoxitin 2gm. i.m. with oral probenecid 1gm.
• This initial treatment to be followed by oral doxycycline 200 mg. b.d. and metronidazole 400 mg. b.d. for fourteen days.
  
• Patients should be reviewed after 72 hours.
• If the condition is mild an IUCD can be left in place.
  
• If it is more severe, it should be removed.
  
• Pelvic inflammatory disease is an absolute contra-indication to the insertion of an IUCD at the time.

GH

Low: short stature, delayed puberty [Treatment: TRH]

High: acromegaly, gigantism [T: somatostatin, dopamine analogues]

PROLACTIN

High: galactorrhea [T: bromocriptine, like DOPAMINE]

ADH/AVP/vasopressin

Low: Central DI, from posterior pituitary problem

High: Nephrogenic DI, ADH V2 receptor bad

Symptoms: high urine output, high osmolarity, low blood volume

Hypophysectomy: won't be secreting ADH so won't reabsorb water so

urinate more

THYROID

Hyper: Grave's Disease, Ab activates TSH receptor, high levels of T3 and T4, low TSH from negative feedback of T3, weight loss, hunger, nervousness, sweat, heat intolerance, high BMR, HR, goiter. Can also be caused by high TRH and TSH levels. [T: PTU]

Hypo: AI destruction of thyroid, low T3 and T4, TSH can be high or low. Weight gain, cold intolerance, low BMR, lethargy, goiter. Can cause cretinism (retardation) in developing fetus. [T: TH replacement]

Hashimoto's: main cause of goiter, AI activity towards thyroid gland, high TSH, low T3, T4

ADRENAL CORTEX

High cortisol: hyperglycemia

Low cortisol: hypoglycemia

High aldosterone: High K secretion, hypokalemia, hypervolemia

Low aldosterone: Low K secretion, hyperkalemia, hypovolemia

High androgens: masculinization of females

Low androgens: loss of pubic hair and libido in females

Addison's Disease: primary adrenal cortex deficiency, all 3 hormones low, also get hyperpigmentation form high ACTH levels and relates MSH levels. [T: H replacement]

Secondary adrenalcortical insufficiency: Low CRH and low ACTH. All 3 hormones low. Mostly normal aldosterone. No hyperpigmentation

Cushing's syndrome: High cortisol causes low ACTH. Obesity. DEX test lowers ACTH

Cushing's disease: High cortisol and high ACTH from pituitary tumor. DEX test does nothing. Central obesity, buffalo hump, striae, hyperglycemia [T: metyrapone blocks cortisol synthesis]

Conn's disease: Primary hyperaldosteronism, via tumor

21-B-hydroxylase deficiency: No aldosterone, cortisol. Shunts to androgens, virilization of females. High ACTH levels. [T: H replacement]

17-A-hydroxylase deficiency: No androgens or cortisol, shunts to aldosterone. Lack of pubic hair and low libido in women, high BP

INSULIN

Diabetes Type I: destruction of pancreatic B cells. Hyperglycemia, FFA, ketoacids, polyurea, thirst

Diabetes Type II: obesity causes, insulin resistance

PTH

Primary hyperPTH: From PTH tumors, high PTH, high cAMP, high blood Ca, stones bones and groans

Secondary hyperPTH: Vitamin D deficiency, high PTH, high cAMP, low calcitriol, low 25(OH)D, low Ca, low phosphate. Lack of vitamin D can lead to RICKETS

HypoPTH: Low PTH, low cAMP, low Ca, high phosphate. [T: Calciotriol]

Chronic renal failure: No calcitriol produced, bone abnormalities, 25 (OH)D in liver normal

PTH peptide: low PTH, high cAMP, high Ca

Description and Symptoms

Facial acne like pimples along with redness, telangiectases and flushing in adults. Usually asymptomatic, though eye involvement may be irritating. Key diagnostic feature is the lack of comedones.

Diagnosis

Clinical.

Pathology

Unknown cause, but higher predisposition in fair skinned female patients. Very common.

Principles of therapy

Avoid triggers (stress, heat, alcohol). Metronidazole gel or the tetracycline class of antibiotics.

Description and Symptoms

Scaly, red plaques that tend to affect the knees, elbows, scalp and sacrum. Most patients have a few small asymptomatic plaques, however some have widespread lesions & /or pruritus. 1% incidence. Possible autosomal dominant inheritance with variable penetrance.

Diagnosis

Clinical appearance, though may confirm with a biopsy.

Pathology

An inflammatory reaction in the skin altered by environmental and genetic factors.

Principles of Therapy

Aggressiveness of therapy must be tailored to clinical situation. Many options available: topical (steroids, calcipotriene, retinoids), ultraviolet light (A&B), and systemic (methotrexate, retinoids, cyclosporine, TNF-alpha inhibitors).

Description and Symptoms

Photodistributed blisters, crusts and erosions that lead to scars and pigmentary changes. May be associated with milia, hypertrichosis and sclerodermoid changes.

Diagnosis

Clinical suspicion confirmed by urine or serum porphyrins.

Pathology

May be associated with viral hepatitis, hormonal therapies, hemodialysis or alcohol intake. Etiology is a defect in the uroporphyrinogen decarboxylase enzyme used in the production of heme.

Principles of Therapy

Complete sun protection extremely important. Treatment of underlying disorder. Phlebotomy and low-dose antimalarials (hydroxychloroquine) are treatment options.

Description and Symptoms

Transient eruption that tends to occur on the trunk of young adults. The first sign is usually a large red scaly plaque (Herald patch), followed later by smaller oval scaly plaques. The eruption lasts 3-8 weeks.

Diagnosis

Clinical, however may be mimicked by syphilis (check RPR).

Pathology

Unknown etiology.

Principles of Therapy

No therapy needed. If symptomatic, topical steroids or UV light may be helpful.

Description and Symptoms

Chronic eruption that affect the mucous membranes, skin and nails. The buccual mucosa often has a lacy white appearance. The skin has itchy reddish-purple flat topped papules with an overlying fine white lacy scale (Wickham’s striae) most commonly seen on the wrists, genitalia and ankles. The nails may be normal, but may be severely dystrophic.

Diagnosis

Clinical suspicion confirmed by biopsy.

Pathology

Unknown. Some drug eruptions can mimic rash. In addition, some studies indicate an association between L.P. and Hepatitis C.

Principles of Therapy

Topical steroids [Clobetasol (strong), Triamcinolone (mod.), Hydrocortisone (mild)] and antihistamines. Drug history and Hepatitis screen may be helpful.

Description and Symptoms

Purpuric papules most often on the lower extremities usually lasting several weeks. Commonly associated with fever, arthralgias and other systemic symptoms including renal involvement. May be idiopathic or associated with a variety of triggering factors (medications, infections, connective tissue disorders).

Diagnosis

Clinical suspicion confirmed by biopsy.

Pathology

Immune complex deposition in the cutaneous vessels leading to vascular destruction and extravasation of RBC’s.

Principles of Therapy

If possible, treatment of the precipitating event or disorder. A variety of medications can be helpful: NSAIDS, Dapsone, Colchicine or Prednisone.

Description and Symptoms

Brown well demarcated macules in areas of chronic sun damage (often the face, neck, upper chest, forearms and hands). Commonly referred to as “liver spots” or “age spots”.

Diagnosis

Clinical. Biopsy is occasionally needed to exclude skin cancer.

Pathology

Increased pigmentation & number of melanocytes in the epidermis. Unlike nevi, no nests are seen.

Principles of Therapy

No treatment needed unless for cosmetic purposes. Laser or LN2 may be used.

Description and Symptoms

Red papules and plaques that form superficial vesicles leading to a characteristic “honey colored” or “golden” crust. The lesions are often asymptomatic, but may be pruritic.

Diagnosis

Clinical suspicion. Bacterial culture can be helpful

Pathology

Superficial infection of the skin with Strep. Pyogenes or Staph. aureus. Often occurs after minor skin trauma.

Principles of Therapy

Topical mupirocin or systemic antibiotics (dicloxacillin, cephalexin, erythromycin).

Description and Symptoms

Recurrent self-limited tender vesicular eruption most often found on the lips and genitalia. Prior to the recurrence, a tingling or burning sensation is usually felt.

Diagnosis

Appropriate history and clinical appearance. Culture or PCR may be used.

Pathology

Herpes Simplex Virus 1 - mostly oral.

Herpes Simplex Virus 2 - mostly genital.

Principles of Therapy

Antivirals (famcyclovir, acyclovir, valacyclovir) taken at the first sign of recurrence may abort or shorten an episode.

Description and Symptoms

Folliculits presents as one or many red papules (and pustules) originating from a hair follicles. Larger, tender nodules are termed furuncles. Multiple follicles may be involved (carbuncle).

Diagnosis

Clinical suspicion. Bacterial culture of the exudates may be helpful.

Pathology

Infection, usually by Staph aureus, of a hair follicle.

Principles of Therapy

Antibacterial soap, antibiotics topical (mupirocin, clindamycin) or systemic (dicloxacillin, cephalexin, erythromycin). PRN I&D. Warm compresses.

Central Rashes.	Etiology	Description
Measles	Paramyxovirus	Rubeola, first disease. Discrete lesions that become confluent as rash spreads from hairline downward, sparing palms and soles. Cough, conjunctivitis.
German measles	Togavirus	Rubella, third disease. Spreads from hairline downward, clearing as it spreads; Forchheimer spots. Adenopathy, arthritis.
Erythema infectiosum	parvovirus B19	Fifth disease. Bright-red "slapped-cheek" appearance ; diffuse lacy reticular rash that waxes and wanes over 3 weeks
Exanthem subitum	herpesvirus 6	Roseola, sixth disease. Diffuse maculopapular eruption (sparing face); resolves within 2 d
Infectious mononucleosis	Epstein-Barr virus	Diffuse maculopapular eruption; periorbital edema (50%); palatal petechiae (25%). Hepatosplenomegaly, pharyngitis, cervical lymphadenopathy, atypical lymphocytosis, heterophile antibody.
Impetigo		Rash on face with discrete vessicles that rupture and form yellow, honey colored crust.
Drug-induced eruption	Drugs	Intensely pruritic, bright-red macules and papules, symmetric on trunk and extremities; may become confluent
Rickettsial spotted fevers	Rickettsia	Eschar at site of bite; maculopapular eruption on proximal extremities, spreading to trunk and face
Lyme disease	Borrelia burgdorferi	Erythema chronicum migrans. Ixodes tick. Expanding "bull's eye" red rash with central clearing, concentric rings. Headache, myalgias, chills, photophobia occurring acutely; CNS disease, myocardial disease, arthritis.
Erythema marginatum	Group A Streptococcus	Rheumatic fever. Erythematous annular papules / plaques evolving / resolving within hours. Pharyngitis preceding polyarthritis, carditis, subcutaneous nodules.
SLE	Autoimmune disease	Macular and papular erythema, often in sun-exposed areas; discoid lupus lesions (local atrophy, scale, pigmentary changes); periungual telangilectasis; malar rash; vasculitis sometimes causing urticaria. Arthritis; cardiac, pulmonary, renal, hematologic, and vasculitic disease.
Pityriasis rosea		Acute solitary, oval, annular lesion of 2-6 cm on the trunk; followed weeks later by eruption of a christmas tree pattern of lesions.

Peripheral Rashes.	Etiology	Description
RMSF	Rickettsia rickettsii	Rash beginning on wrists and ankles and spreading centripetally; palms and soles; blanchable macules  petechiae. Headache, myalgias, abdominal pain.
Secondary syphilis	Treponema pallidum	Copper-colored, scaly papular eruption, diffuse but prominent on palms and soles; rash never vesicular; condyloma latum.
Hand-foot-and-mouth disease	Coxsackievirus A16	Tender vesicles, erosions in mouth; 0.25-cm papules on hands and feet
Bacterial endocarditis	Streptococcus, Staphylococcus, etc.	Subacute: Osler's nodes (tender pink nodules on finger toe pads); petechiae on skin ; splinter hemorrhages. Acute: Janeway lesions (painless erythematous or hemorrhagic macules on palms and soles). New heart murmur.
Erythema multiforme	Drugs, infection…	i.e., Stephens-Johnson. Target lesions surrounded by clearing. Symmetric on knees, elbows, palms and soles.

• Macules are flat lesions defined by an area of changed color (i.e., a blanchable erythema).
• Papules are raised, solid lesions <5>
• Plaques are lesions >5 mm in diameter with a flat, plateau-like surface.
• Nodules are lesions >5 mm in diameter with a more rounded configuration.
• Wheals (urticaria, hives) are papules or plaques that are pale pink and may appear annular (ringlike) as they enlarge; classic (nonvasculitic) wheals are transient, lasting only 24 to 48 h in any defined area.
• Vesicles (<5>5 mm) are circumscribed, elevated lesions containing fluid.
• Pustules are raised lesions containing purulent exudate; vesicular processes such as varicella or herpes simplex may evolve to pustules.
• Nonpalpable purpura is a flat lesion that is due to bleeding into the skin.
• If <3>
• If >3 mm, they are termed ecchymoses.
• Palpable purpura is a raised lesion that is due to inflammation of the vessel wall (vasculitis) with subsequent hemorrhage.

Description and Symptoms

Small to large subcutaneous nodules with an overlying plugged follicular opening (punctum) almost anywhere on the body. Occasionally inflamed due to traumatic rupture of the cyst sack or superinfection.

Diagnosis

Clinical diagnosis

Pathology

Blocked follicular opening leading to accumulation of degenerated hair in the follicle (like a balloon)

Principles of Therapy

No therapy indicated unless for cosmetically bothersome or symptomatic (repeatedly inflamed/tender). Surgical removal is the only option.

DISEASES

All diseases caused by dermatophytes are called tinea coming from the Latin word for worms. That’s because the Romans thought it was worms getting into your skin. They are then named after the place they infect so T. capitas is the head, T. corporis – body, T. cruris – crotch, T. manum – hand, T. pedis – feet, T. unguium – nails. Over 50% of people will be infected in their lifetime; it is the second most common disease, and over $200,000,000/yr are spent on cures.

1. T. pedis  the most common tinea (30- 70%). It starts off mild and then can go into remission or into secondary bacterial infection which looks really really gross. T. pedis only started being such a problem in the last 200 years because of people wearing tight, non-airy shoes. It’s more common in adults and in people with a genetic predisposition. Caused by T. rubrum, mentagrophytes, and E. floccosum. The treatment is creams, and if that don’t work then systemic antifungals.

2. T. unguium  starts off in a corner and spreads, sometimes even to other toes. Usually caused by T. rubrum. The only effective treatment is systemic antifungals for several months and monitor liver functions. 5-10% of the population get it.

3. T. capitas  scalp infection, usually caused by microsporum and trichophyton. Mostly affects young people and African Americans. The incidence has been decreasing, probably due to better sanitary conditions. The infection smells like urine and mouse droppings. There are infections that are anthrophilic and live inside the hair shaft and other live on the outside. They weaken the hair and cause it to break. Prevention includes avoiding oiling or braiding hair, not sharing combs or hats, going to clean barbers, avoid overcrowding, skin trauma, and animals. Treatments over the years have been really weird. In Paris, they covered the head with tar and then pulled it off. Then they used X-rays but that led to baldness and brain tumors. Now we use azoles for 2-4 weeks or griseofulvin for 6-8 weeks.

4. 
   

5. T. cruris  affects the groin and perineum, usually caused by T. rubrum, and E. floccosum. Usually men get it. It spares the penis and scrotum. It can be prevented by using loose cotton clothing, sterilize towels and underpants, and losing weight. It’s treated with topical and systemic antifungals.

6. T. corporis  caused by T. rubrum, and T. mentagrophytes. People have it and scratch the lesions and pass it on to other parts of the body. The middle of the lesion is smooth and the edge is bumpy due to an immune response.

There are skin infections that can be confused with dermatophytic infections. These include T. versicolor is caused by yeast. It makes someone have spots that are darker or lighter than thir skin and comes out in the sun. Candida will be dealt with later. Sebhorreic dermatitis is probably caused by an exaggerated T-cell response to yeast. Eczema is an immune response seen in 10-20% of the population, especially babies. Psoriasis is scaling, thickening, and inflammation of the skin.

Diagnosis:

The doctor takes a scraping or clips the nail  adds KOH and ink, this melts keratin, but don’t harm the hyphae  adds fluorescent coloring  if there’s fungi they stand out under UV light. In the lab it grows slow at low temperatures. Chloramphenicol is added to kill bacteria and cyclohexinide to kill fast growing fungi. Then the lab looks at the plates, but interpretation is varied and experience is needed. On DTM plates, dermatophytes form red halos because they change the pH. An important thing to know for the boards is that they used to use a wood lamp (which is a UV light) and hold it to the hair. If the hair fluoresces then it’s a fungal infection.

Intubation only

(oxygenation and ventilation are adequate but the patient needs a secure airway)
Threatened airways obstruction;e.g., deep coma
Definite airways obstruction;e.g., laryngeal edema, tracheal tumor

Either indication must be based solely on the clinical examination, although arterial blood gas measurement is often helpful to assure that mechanical ventilation is not necessary.


Intubation and mechanical ventilation
(oxygenation and/or ventilation are not adequate)

*Apnea

*Impaired alveolar ventilation (as assessed by PaCO2) when accompanied by one or more of the following:
a. Depressed mental status
b. Increasing fatigue
c. Reduced PaO2 that cannot otherwise be corrected
d. Severely deranged pH that cannot otherwise be corrected
e. Compromise of upper airways (e.g., by secretions)

*Low PaO2 (e.g., less than 60 mm Hg): a. that cannot be improved with an FIO2 less than 0.50, and b. that is causing symptoms or seriously impairing bodily function

SECOND BRANCHIAL ARCH: All muscles of facial expression are derived from the second branchial arch and are innervated by branches of the Facial Nerve (VII).

o Fractures that affect the facial skeleton:

1. La Fort 1: A horizontal fracture through the maxilla, at the base of alveolar process (i.e. at the top of the upper teeth).

§ The alveolar process of the maxilla and upper teeth come of as a unit.

§ The rest of the maxilla remains attached to the zygomatic bone.

2. La Fort 2: Complete separation of the maxilla. Essentially, the nose is separated from the facial skeleton.

§ Zygomatic bone remains intact and separated from Maxilla.

3. La Fort 3: Zygomatic bone separates from the frontal bone. Essentially, the entire face breaks lose from the cranium.

§ The orbits drop down, causing double vision.

o FACE LACERATIONS: Because facial skin is loose, lacerations in the face tend to gape. Injuries in the face tend to swell more than other tissues.

o GALEA APONEUROTICA: Superficial fascia of the scalp. The frontalis muscle inserts into the Galea Aponeurotica.

o STARVATION: The Buccal Fat Pad, directly deep to the Buccinator Muscle, and the Retro orbital Fat Pad are the last fat stores to be used when energy is needed. Thus depletion of these fat-pads (sunken eyes and hollowed out cheeks) indicates starvation.

THE FACIAL ARTERY supplies blood to the superficial structures of face.

• The facial artery is one of the principle branches given off the External Carotid.

• Course:
• It is given off just deep to the angle of the mandible.
• It crosses the inferior border of the mandible just anterior to the masseter muscle.
• Once it’s on the anterior surface of the face, it goes up the cheek, past the angle of the mouth, and heads toward the inner canthus (medial corner) of the eye.
• A Facial Artery Pulse can be palpated as the artery crosses the mandible just anterior to the masseter muscle.
• Branches:
• Superior Labial Branch above mouth
• Has anastomoses with the Infraorbital Artery
• Inferior Labial Branch below mouth
• Angular Artery heads up to the nose
• Has anastomoses with the Ophthalmic Artery
Lateral Nasal Branch
• 
  

SUPERFICIAL TEMPORAL ARTERY: The terminal branch of the External Carotid.

• Goes straight up the temporal region of the skull.
• Branches:
• Frontal Branch
• Parietal Branch.
• Transverse Facial Artery crosses Masseter muscle
• Anesthesiologists use it to take a pulse. It is found just anterior to the ear, superficial to the zygomatic arch.
  

VEINS OF THE FACE:

1. Venous Channels:

• Facial Vein provides the major venous drainage ------> Internal Jugular Vein.
• Facial vein is formed from the Supraorbital + Supratrochlear Veins ------> Angular Vein (comes down from medial canthus of eye) ------> Facial Vein.
• Facial vein then joins with the Submental Vein to lead to the Internal and External Jugular Veins.
• Retromandibular Vein is formed by the union of the Superficial Temporal Vein and Maxillary Vein.
• It then joins with the Posterior Auricular Vein to form the External Jugular Vein.
• It also gives off a branch back to the facial vein ------> Internal Jugular.

2. Anastomoses with Cranial Fossa: Clinically important collateral circulation with the dural sinuses occurs at two places:

• Deep Facial Vein is a communication between the Facial Vein and the Pterygoid Plexus.
• Superior Ophthalmic Vein is a communication between the Facial Vein and the Cavernous Sinus.

3. Dangerous Area of Face: A triangle approximately covering the nose and maxilla, and going up to the region between the eyes. Superficial Veins communicate with dural sinuses in this region.

• The Facial Vein has no valves. Backflow can cause infection to get into the dural sinuses, through the Deep Facial Vein (via pterygoid plexus) and Superior Ophthalmic Vein (via Cavernous Sinus)
  

LYMPHATIC DRAINAGE:

1. Parotid Nodes: Superficial and deep set.

2. Submandibular Nodes

3. Retroauricular Nodes